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Effect of miRNA26b knockout on vascular calcification [scRNA-seq]

ABSTRACT: Vascular calcification is the abnormal deposition of calcium phosphates within the blood vessels. Although it significantly contributes to the development of cardiovascular disease, much remains unknown about the mechanisms driving this process. Recent advances have shown that microRNAs (miRNAs) could be critical in regulating the biological processes driving vascular calcification. Here, we investigated whether miRNA-26b (miR-26b) could regulate vascular calcification. By performing scRNA-seq of the aorta of miR-26b knockout (miR-26bKO) mice, we identified cell-specific targets and demonstrated that components of the BMP signalling pathway are dysregulated in the aortic cell types.

ORGANISM(S): Mus musculus

PROVIDER: GSE281028 | GEO | 2025/11/14

REPOSITORIES: GEO

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Effect of miRNA26b knockout on vascular calcification [RNA-seq]

Project description:Vascular calcification is the abnormal deposition of calcium phosphates within the blood vessels. Although it significantly contributes to the development of cardiovascular disease, much remains unknown about the mechanisms driving this process. Recent advances have shown that microRNAs (miRNAs) could be critical in regulating the biological processes driving vascular calcification. Here, we investigated whether miR-26b could regulate vascular calcification. By performing bulk RNA-seq of the aorta of miR-26bKO mice, we identified cell-specific targets and demonstrated that BMP signalling is dysregulated in aortic cells.

2025-11-14 | GSE281279 | GEO

Endothelial BMP6 Drives Hemodynamic-Dependent VSMCs Calcification in Carotid Atherosclerosis

Project description:Carotid atherosclerosis (CAS) is a major contributor to ischemic stroke, with vascular calcification driving disease progression. However, the molecular mechanisms driving vascular calcification in CAS remain unelucidated. Previous studies have confirmed that bone morphogenetic proteins (BMPs) play essential roles in calcification; however, the regulatory mechanisms of BMP6 signaling in vascular calcification remain unclear. This study aimed to investigate the role of BMP6 in vascular calcification in CAS and the underlying mechanisms. A subset of endothelial cells (ECs) with high BMP6 expression, which interacted with specific vascular smooth muscle cells (VSMCs) via the BMP signaling pathway, was identified using single-cell RNA sequencing of human CAS plaque samples. In vitro experiments demonstrated BMP6-induced osteogenic differentiation of VSMCs. Moreover, BMP6 activated the p-SMAD1/5/8 signaling pathway by binding to the ACVR1–BMPR2 receptor complex, and pharmacological inhibition of this pathway attenuated osteogenic differentiation. Experimental results from endothelium-specific BMP6 knockout (BMP6ECKOApoE-/-) and overexpression (AAV-Cdh5-BMP6) mice confirmed that BMP6 exacerbated vascular calcification, whereas its knockdown reduced calcific lesions. Additionally, disturbed flow conditions upregulated BMP6 expression by suppressing Krüppel-like factor 4 and linking hemodynamic forces to BMP6-mediated calcification. These findings suggest that BMP6 is a key regulator of vascular calcification in CAS, driven by EC–VSMC interactions and hemodynamic stress

2025-10-03 | GSE309462 | GEO

The Pharmacological Effect and Mechanism of Lanthanum Hydroxide on Vascular Calcification Caused by Chronic Renal Failure Hyperphosphatemia

Project description:Objective: To investigate the treatment and mechanism of lanthanum hydroxide on hyperphosphate-induced vascular calcification in chronic renal failure. Methods: Develop a rat model of CKD hyperphosphatemia. Rats were randomly allocated to the model, lanthanum hydroxide, lanthanum carbonate, Calcium carbonate groups. Determination of serum biochemical indicators and the determination of pathological analysis of kidney tissue, Von Kossa staining and CT scan on the aortic vessels. The proteomic analysis of aortic tissue in Vivo. A calcified VSMCs model was established. The calcium content and ALP activity were measured. RT-PCR measures the mRNA expression level of SM22α, Runx2, BMP-2 and TRAF6. Western Blot measures the protein expression level of SM22α, Runx2, BMP-2, TRAF6 and NF-κB. Results: Through the detection of serum biochemical indicators and pathological analysis of kidney tissue, it can be summaryed that lanthanum hydroxide has the effect of delaying the progression of renal failure and protecting renal function. We found that the administration of lanthanum hydroxide delayed the development of vascular calcification induced by hyperphosphatemia in CKD. It can be concluded that lanthanum hydroxide may affect vascular calcification through the NF-κB pathway. , To deal with Lanthanum chloride (LaCl3) inhibited phosphate induced calcification, osteo-/chondrogenic transdifferentiation, and NF-κB signaling in cultured VSMCs. Lanthanum hydroxide significantly reduces the expression of Runx2, BMP-2, TRAF6 and NF-κB. Conclusion: Lanthanum hydroxide has a protective effect on the kidneys, and can delay the development of vascular calcification by reducing serum phosphorus concentration.

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Indoxyl sulfate and p-cresyl sulfate directly promote vascular calcification via activation of inflammation and coagulation pathways

Project description:Vascular calcification contributes to high cardiovascular mortality in chronic kidney disease (CKD) patients. An association between the uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (PCS) and cardiovascular disease has been suggested. This study provides strong etiological evidence for indoxyl sulfate and p-cresyl sulfate as major contributors to vascular calcification in chronic kidney disease patients. Continuous exposure to indoxyl sulfate or p-cresyl sulfate in rats with chronic kidney disease promotes moderate to severe calcification in the aorta and peripheral vessels. Unbiased proteomic analyses of arterial samples coupled to functional bioinformatics annotation analysis revealed that calcification events were associated with acute phase response signaling, coagulation and glucometabolic signaling pathways, while escape from toxin-induced calcification was linked with liver X receptors and farnesoid X/liver X receptor signaling pathways. Activation of inflammation and coagulation pathways in the arterial wall plays a pivotal role in toxin-induced calcification and strongly associates with hyperglycemia and insulin resistance. These findings reveal new perspectives to establish novel therapeutic targets to prevent, halt progression or cure vascular calcification.

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Project description:This study aimed to identify small molecules that inhibit vascular calcification with computational approach. To examine the mechanism of calcification inhibition, proteomics analysis was performed using aorta tissue samples to clarify therapeutic target.

2022-02-17 | PXD029963 | Pride

microRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification, the ectopic deposition of calcium in blood vessels, develops in association with various metabolic diseases and atherosclerosis. Because it often causes stiffness and remodeling of the blood vessels, vascular calcification increases morbidity and mortality. Both miRNA and mRNA microarrays (Series GSE74755) were performed with rat VSMCs and reciprocally regulated pairs of miRNA and mRNA were selected after bioinformatic analysis.

2019-12-31 | GSE130486 | GEO

Reactivation of TET2 reverses vascular smooth muscle cell osteogenic differentiation and prevents medial aortic calcification

Project description:Cardiovascular diseases often manifest with vascular calcification. Vascular calcification is an active process orchestrated by contractile vascular smooth muscle cell (VSMC) phenotypic switch to an osteoblast-like cell. Here, we identified that the DNA demethylase, Tet2 (Ten-eleven translation 2), safeguards VSMCs from transitioning into the osteogenic lineage and loss of Tet2 promotes development and progression of vascular calcification. Tet2 was among the most significantly downregulated epigenetic markers in calcified aortas. VSMC-specific loss of Tet2 promoted VSMC osteogenic differentiation and enhanced vascular calcification as evidenced histologically, molecularly, and hemodynamically. In vivo studies further indicated that Tet2 inhibits calcification-associated VSMC apoptosis and medial thinning. Notably, calcified regions were enriched in a Trem2hi (triggered receptor expressed on myeloid cells 2) macrophage subpopulation. Intervention studies using high-dose ascorbate to enhance Tet2 enzymatic activity resulted in significantly reduced medial aortic calcification and improved aortic structural integrity in mice. Ascorbate treatment in human aorta organ cultures was sufficient to reduce calcification development in diseased tissues, and restore contractile properties to the calcified aorta. This study highlights the potential clinical impact of modulating Tet2 activity in managing cardiovascular disorders associated with vascular calcification.

2025-07-01 | GSE294266 | GEO

mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC. Calcification was induced in rat aorta vascular smooth muscle cells with inorganic phosphate (Pi). Total RNA were extracted from the cells 3 and 6 days later. mRNA profile of the sample was compared with normal control.

2015-11-07 | E-GEOD-74755 | biostudies-arrayexpress

Hypotaurine reduces glucose-mediated vascular calcification

Project description:To study the underlying molecular mechanisms driving vascular calcification, we analyzed the transcriptome of calcium-phosphate calcified human coronary aortic smooth muscle cells cultured with zero, low, and high glucose for 3 days.

2025-07-16 | GSE283693 | GEO

Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.

2024-05-14 | GSE254075 | GEO

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